Autoimmune disease arises from an inappropriate immune response of the body against certain tissues present in the body. This autoimmune response may be restricted to certain organs, for example the pancreas as in diabetes mellitus, or may affect only certain membranes of certain tissues and organs. One of the functions of the immune system is to protect the body by responding to invading microorganism, such as viruses or bacteria, by producing antibodies or sensitized lymphocytes. Under normal conditions, an immune response cannot be triggered against the cells of one's own body. However, autoimmune diseases are characterized in that the body's immune system may make a mistake and attack the cells they are meant to protect. Therefore, autoimmune disease encompasses a broad category of related diseases in which the body's immune system attacks its own tissue.
An autoimmune disease is any disease caused by immune cells that become misdirected at healthy cells and/or tissues of the body. Currently, autoimmune disease affects 3% of the U.S. Population and likely a similar percentage of the industrialized world population. Autoimmune diseases are characterized by T and B lymphocytes that aberrantly target self-proteins, -polypeptides, -peptides, and/or other self-molecules causing injury and or malfunction of an organ, tissue or cell type within the body. Thus, autoimmune disease occur when there is some interruption of the normal control process, which allows lymphocytes to avoid suppression, or when there is an alteration in some body tissue so that it is no longer recognized as “self” and thus is attacked. The exact mechanism causing autoimmune disease may differ but may be triggered by many factors including: bacteria, viruses, toxins, drugs, and genetic predisposition.
Autoimmune diseases include diseases that affect specific tissues as well as diseases that can affect multiple tissues. The characteristic feature of tissue-specific autoimmunity is the selective targeting of a single tissue or individual cell type. However, certain autoimmune diseases that target ubiquitous self-proteins can also affect specific tissues.
Particular autoimmune diseases are often classified into organ-specific disorders and non-organ-specific types. For example, Hashimoto's disease affects the thyroid gland, Addison's disease affects the adrenal glands, and Type 1 diabetes mellitus affects the pancreas. Examples of non-organ-specific autoimmune diseases include rheumatoid arthritis, systemic lupus erythematosus and dermatomyositis. More than 30 autoimmune diseases are presently known, including rheumatoid arthritis, insulin-dependent diabetes mellitus, multiple sclerosis, myasthenia gravis, systemic lupus erythematosis, and scleroderma. Additional nonlimiting examples of autoimmune disease include: acute disseminated encephalomyelitis, Addison's disease, amyotrophic lateral sclerosis, autoimmune hepatitis, autoimmune lymphoproliferative syndrome, Berger's disease, Blau syndrome, certain types of cancer, celiac disease, Chagas disease, chronic recurrent multifocal osteomyelitis, Churg-Strauss syndrome, Cogan syndrome, cold agglutinin disease, Crohn's disease, Cushing's syndrome, Diabetes Mellitus type 1, Evan's syndrome, Grave's disease, Hashimoto's encephalopathy, Kawasaki's disease, Lou Gehrig's disease, Meniere's disease, multiple sclerosis, neuromyotonia, ocular cicatricial pemphigoid, psoriasis, psoriatic arthritis, Reynaud phenomenon, Reiter's syndrome, restless leg syndrome, rheumatoid arthritis, Sjogren's syndrome, temporal arteritis, transverse myelitis, vaculitis, and Wegener's granulomatosis.
Diabetes mellitus is a generic term for metabolic disorders characterized by persistence of a hyperglycemic state due to the deficiency of insulin action. Generally, diabetes mellitus is classified roughly into insulin-dependent diabetes mellitus (“IDDM”) and non-insulin-dependent diabetes mellitus (“NIDDM”). One form of IDDM includes type 1 diabetes mellitus (“T1D”), which is a form of diabetes mellitus that results from the autoimmune destruction of insulin-producing beta cells of the pancreas.
Insulin is a biological material that suppresses elevated blood glucose levels. Insulin is a hormone secreted by the pancreas that can promote carbohydrate metabolism in the liver and enhance the uptake of glucose into muscle cells and fat cells in order to lower an elevated blood glucose level. A lack of insulin, which leads to an increase in blood and urine glucose, is observed both while the beta cells of the pancreas are being destroyed and when all the beta cells have been destroyed. As such, diabetes mellitus is characterized by recurrent or persistent hyperglycemia.
T1D may be induced by many different factors including genetic factors, environmental factors, dietary factors, an individual's overall susceptibility, diabetogenic triggers and/or exposure to a driving antigen. T1D is currently understood to be a polygenic disease, meaning that different genes can contribute to the onset of T1D.
Typical symptoms of T1D include polyuria (frequent urination), polydipsia (increased thirst), xerostomia (dry mouth), polyphagia (increased hunger), fatigue and weight loss. Often times, untreated T1D can lead to diabetic ketoacidosis. Diabetic ketoacidosis is a potentially life-threatening complication that occurs when the body experiences a shortage of insulin and thus begins breaking down fatty acids for energy. The breakdown of the fatty acids produces acidic ketone bodies that cause many of the symptoms described herein.
Another form of diabetes mellitus includes T2D, which is a type of diabetes mellitus in which hyperglycemia is manifested due to insufficient insulin secretion and insulin resistance caused by uncertain and diverse factors such as aging, stress, and diet. T2D is characterized as NIDDM. Typically, about 90% of all individuals with diabetes mellitus fall under NIDDM.
Rapid increases in blood glucose levels after meals and its continuance for many years is known to exacerbate diabetes mellitus. Exacerbation of diabetes mellitus is often accompanied by promotion of angiopathy, which can lead to development of neurosis, nephropathy and retinopathy and to further complications of myocardial infarction and apoplexy.
For individuals prone to developing or suffering from diabetes mellitus often, certain types of diet and exercise therapies are adopted. Adopting certain exercise and diet patterns can help stabilize blood glucose levels and may improve overall carbohydrate metabolism.
Evidence has shown that tight glycemic control is a major factor in the prevention of complications associated with diabetes mellitus. However, currently available agents generally fail to maintain adequate glycemic control in the long term due to progressive deterioration of hyperglycemia, resulting from progressive loss of pancreatic cell function. Therefore, optimal glycemic control by drugs, therapeutic regimens, nutritional supplements and/or nutritional compositions is an important approach for the treatment of diabetes mellitus. While diabetes mellitus may be treated by insulin or the administration of oral hypoglycemic drugs, there is a need for a safe and effective nutritional supplement or nutritional composition for reducing the incidence of diabetes mellitus.
Autoimmune diseases may be treated with immunosuppressive agents, hormone replacement therapy or blood transfusion, in the case of autoimmune blood disorders. These treatments include several unwanted side effects and can be costly for the target subject. Secondly, when administering immunosuppressive agents, there is a delicate balance between diminishing the activity of the immune system while allowing the immune system's ability to fight disease in general. Further, immunosuppressive agents may cause unwanted side effects such as bone loss and/or bone and tissue deterioration.
Accordingly, the present disclosure provides a nutritional composition comprising a peptide component that may reduce the incidence of autoimmune disease. Further, the present disclosure provides a nutritional composition comprising a peptide component that may reduce the incidence of T1D and T2D by providing a nutritional composition including the peptide component disclosed herein to target subject.